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| the branch of medical science that studies the nature, causes, and effects of diseases. |
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| abnormal redness of the skin resulting from dilation of blood vessels (as in sunburn or inflammation) |
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| pertaining to a female that has not had offspring |
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| an abnormal passage leading from a suppurating (discharge pus) cavity to the body surface |
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| crack: a long narrow opening |
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Any condition of body or mind that "decreases the chances of survival" of an individual or species.
Exceptions: Sickle Cell: an abnormal red blood cell that has a crescent shape and an abnormal form of hemoglobin. Achondroplasia: an inherited skeletal disorder beginning before birth; cartilage is converted to bone resulting in dwarfism. |
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| Some “diseases” aren’t real |
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Nostalgia: ex. wanting to go home. Drapetomania: a supposed mental illness described by American physician Samuel A. Cartwright in 1851 that caused black slaves to flee captivity. Masturbation: a mental disease that must be corrected. |
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| SOME DISEASES HAVE DISAPPEARED |
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Due to our efforts --small pox
Due to erroneous concepts (characterized by an error, inaccurate) 1. Glenard’s Disease: an abnormally downward position of the intestines in the abdominal cavity. Was really gravity.
2. Status Thymicolymphaticus: the triangular shape, a thyroid. They would radiate the thyroid, would cause cancer for them later. Carcinoma of the thyroid (25 years later). |
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| Normal Cell --> Cell Death |
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| Normal Cell Adaptation Irreversible Injury Necrosis (really response to cell death, always pathologic) or Apoptosis. Oncrosis: real cell death. |
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| RESPONSES OF CELLS TO INJURY |
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NATURE OF INJURY RESPONSES OF CELLS NONLETHAL STIMULI ADAPTATION Increa. stimuli(e.g.hormones) hyper-plasia/trophy Decrea. nutrients/ stimuli atrophy Chronic irritation metaplasia DECRES. OXYGEN/CHEMICALS/INFEC. INJURY Acute & transient reversible( swelling/ fat) Progressive/ severe(includes DNA) irreversible death necrosis/apoptosis/ autophagy METABOLIC(genetic/acquired),CHRONIC INJURY CELL ACCUMULATIONS CALCIFICATION CUMULATIVE SUBLETHAL CELLULAR AGING |
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First line of defense Failure --> reversible or irreversible cell injury
1. atrophy: (less exercise, smaller muscle cells). 2. hypertrophy 3. hyperplasia 4. metaplasia |
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a decrease in size of body tissues.
2. physiologic (functions of an organism) or pathologic (diseased, clotting that cuts off blood flow) 3. active processes 4. often reversible |
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| abnormal increase in body organs. |
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| abnormal increase in number of cells. |
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Reduced metabolic activity --> decreased protein synthesis
Nutrient deficiency or disuse --> 1.) activation of ubiquitin - proteasome pathway 2.)accelerated proteolysis in catabolic conditions (including cachexia )
May be accompanied by autophagy which may produce residual bodies (brown atrophy, lipids that have not been dissolved completely) |
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1. Reduced metabolic activity --> decreased protein synthesis 2. Nutrient deficiency or disuse --> activation of ubiquitin - proteasome pathway also may --> accelerated proteolysis in catabolic conditions (including cachexia (fatigue)) 3. May be accompanied by autophagy --> may produce residual bodies |
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MECHANISMS OF ATROPHY
Order to Residual Bodies |
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-Autophagy: Digestion of the cell's own organelles.
Organelle ER-derived membrane Early Autophagic body Lysosomal Hydrolase Tubulovesicular body Late Autophagic body Residual body |
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| pigmented lipid granules that accumulates in several body tissues (Residual bodies) |
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| CAUSES OF PATHOLOGIC ATROPHY |
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1.disuse 2.neurotrophic changes 3.decreased blood supply 4.nutrition (marasmus / cachexia /Kwashiorkor) 5.loss of endocrine stimulation 6. aging 7. pressure 8. x-ray 9. Immunologic |
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-lack of protein-caloric (a little fatty). -Skinny |
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| Cachexia=wasting that can’t be reversed nutritionally (their heads are huge. A reduction of cells, and also a reduction is lipids), break down of fats. |
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-Decrease in proteins. -Big stomach. -Excess of Albumin. -Ascites: accumulation of serous fluid in peritoneal cavity. |
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| accumulation of serous fluid in peritoneal cavity (abdomen). |
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| “CELLULAR CHANGES” IN ATROPHY |
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Identical in all of these settings Early –cells have diminished function but aren’t dead Atrophy caused by decreased blood supply may apoptosis Apoptosis also contributes to effects on endocrine organs after hormone withdrawal |
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| Decrease in brain material |
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| Hydronephrosis of the Kidney |
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| Atrophy due to pressure. Marked dilation of the pelvis and calyces and thinning of the Renal Parenchyma. |
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ATROPHY OTHER THINGS THAT ARE SMALL |
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APLASIA & AGENESIS = failure of development of primordium
HYPOPLASIA—incomplete development
ATRESIA—absence of an opening e.g. trachea |
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ATROPHY EXTRACELLULAR TISSUES |
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NOT SPARED—severity depends in part on cellular metabolism Immobilized limbs (reduced muscle --> 1.)loss of proteoglycans in articular cartilage 2.)decr. strength of ligaments
Osteoporosis (Osteopenia) = loss of bone mass, not loss of calcium |
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| Osteoporosis (Osteopenia) |
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loss of bone mass not loss of calcium. loss of bone mass not loss of calcium. Either you get rid of the Osteoblast, or you make the Osteoclast does more (increased activity). One way is lack of bone use. Lack of physical activity and aging. Nutrition is also important. |
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TYPE OF TISSUE DETERMINES REVERSIBILITY 1. motor de-nervation of skeletal muscle 2. fat |
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1. return of function if repaired in 3-5 weeks, useless to repair after 20-24 months 2. complete (reversibility?) |
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| INCREASE CELL, TISSUE OR ORGAN SIZE |
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MECHANISMS Hypertrophy=increase in size Hyperplasia=increase in number -hormonal -compensatory |
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INCREASE CELL, TISSUE OR ORGAN SIZE -CELLULAR CHANGES IN HYPERTROPHY AND HYPERPLASIA |
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CYTOPLASM INCREASED MORE BASOPHILIA= more protein NUCLEOLUS ENLARGED=more ribosomes NUCLEUS ENLARGED BUT LESS BASOPHILIC=chromatin dispersed = increased DNA transcription |
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| CELLULAR CHANGES IN HYPERTROPHY AND HYPERPLASIA |
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CYTOPLASM INCREASED MORE BASOPHILIA (the tendency of cells to stain with basic dyes) = more protein NUCLEOLUS ENLARGED = more ribosomes NUCLEUS ENLARGED BUT LESS BASOPHILIC = chromatin dispersed = increased DNA transcription |
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| PATHWAYS TO HYPERTROPHY / HYPERPLASIA |
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INCREASED FUNCTIONAL DEMANDS ENDOCRINE STIMULATION PATHOLOGIC HYPERPLASIA COMPENSATORY HYPERPLASIA EXCESSIVE NUTRITION INCREASED BLOOD FLOW MECHANICAL FACTORS |
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| CARDIAC HYPERTROPHY REVERSIBILITY |
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1. REVERSIBLE INITIALLY
2. MUSCLE MASS AND RNA = NORMAL
3. BUT DNA AND FIBROSIS DON’T CHANGE à CELLS APPEARING TO HAVE INCREASED NUCLEAR SIZE
4. AT SOME POINT FIBROSIS (The replacement of normal tissue with scar tissue) OCCURS --> DECREASED COMPLIANCE
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-Right sided Cardiac failure: most likely cause is Left sided Cardiac failure.
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1.Almost entirely reversible.
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•P-450 central (of the liver) – possible results
–Detoxification
–More injurious
•Polymorphisms (the genetic variation within a population that natural selection can operate on) influence P-450 --> varied sensitivity of individuals to particular drugs
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HYPERPLASIA
PATHOLOGIC--EXAMPLES
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1. Excess of hormones or growth factors e.g. endometrium
2.Characteristic of viral infections e.g.HPV
1&2DISTINCT FROM CANCER BUT PROVIDES FERTILE SOIL FOR CANCER
3.Chronic Renal failure ® decreased serum Ca2+ ® parathyroid hyperplasia
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1.You decrease the variety of the cells. Too many of the same type of cell.
-No fats
-1 cell type predominates.
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-a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus.
-Polyps: providing the extra surface area.
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PHYSIOLOGIC HYPERPLASIA
Terminal Ductal Lobular Unit (TDLU). |
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| During pregnancy, branching of terminal ducts results in more numerous TDLUs, and the number of acini per TDLU increases. |
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PHYSIOLOGIC HYPERPLASIA
Acini
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| The sac-like part of the milk-producing glands in the breast. These are also called lobules. |
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| Counterbalancing, neutralizing, making compensation for some injury or lack. |
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consists on the surgical resection of the liver. The term is often employed for the removal of the liver from a liver transplant recipient.
1.Priming à Proliferation à Growth Inhibition
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